Investigation of manganese transport system in neuronal cells

锰是一种必需元素，但暴露在过量的锰中会引起类似帕金森氏症的症状。虽然许多转运体可能参与锰的摄取，但关于神经系统中锰的转运，只有DMT1和转铁蛋白受体的作用被研究过。为了证实DMT1的贡献，我们首先检测了DMT1 siRNA的作用。因此，导入DMT1的siRNA抑制了人神经母细胞瘤SH-SY5Y细胞对锰的摄取。接下来，我们重点研究了锌转运蛋白ZIP8和ZIP14，它们既可以转运锰，也可以转运锌和镉。在SH-SY5Y细胞和小鼠海马HT22细胞中，导入ZIP14的siRNA均可抑制对Mn和Cd的摄取，但ZIP8不能抑制它们的摄取。这些结果表明，除DMT1外，ZIP14可能在神经细胞的锰转运中发挥重要作用。

Manganese(Mn) is an essential element, but exposure to excess amount of Mn causes symptoms similar to Parkinson's disease. Although several transporters may be involved in Mn uptake, only the role of DMT1 and transferrin receptor have been examined regarding Mn transport in nervous systems. To confirm the contribution of DMT1, we first examined the effects of DMT1 siRNA. As a result, the uptake of Mn in human neuroblastoma SH-SY5Y cells was suppressed by introduction of siRNA of DMT1.Next, we focused on zinc transporters, ZIP8 and ZIP14, which can transport Mn as well as Zn and Cd. The uptakes of Mn^<2+> and Cd^<2+> were suppressed by the introduction of siRNA of ZIP14, but not by ZIP8, in both SH-SY5Y and mouse hippocampus HT22 cells. These data suggest that ZIP14 in addition to DMT1 might play an important role in Mn transport in neuronal cells.